Evidence map›Paper›PMID 18566685›Full record

ArticleMediators of inflammation2008

Prolonged classical NF-kappaB activation prevents autophagy upon E. coli stimulation in vitro: a potential resolving mechanism of inflammation.

Silke Schlottmann, Franziska Buback, Bettina Stahl, Rainer Meierhenrich, Paul Walter, Michael Georgieff, Uwe Senftleben

Abstract read
In one paragraph

Article in Mediators of inflammation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Mechanism and medical implications of mammalian autophagy.Nature reviews. Molecular cell biology · 2018
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. AcanthopanaxMediators of inflammation · 2016
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Silke SchlottmannDepartment of Anesthesiology and Intensive Care, University of Ulm, 89075 Ulm, Germany.
Franziska Buback
Bettina Stahl
Rainer Meierhenrich
Paul Walter
Michael Georgieff
Uwe Senftleben

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of NF-kappaB is known to prevent apoptosis but may also act as proapoptotic factor in order to eliminate inflammatory cells. Here, we show that classical NF-kappaB activation in RAW 264.7 and bone marrow-derived macrophages upon short E. coli coculture is necessary to promote cell death at late time points. At 48 hours subsequent to short-term, E. coli challenge increased survival of NF-kappaB-suppressed macrophages was associated with pattern of autophagy whereas macrophages with normal NF-kappaB signalling die. Cell death of normal macrophages was indicated by preceding downregulation of autophagy associated genes atg5 and beclin1. Restimulation of macrophages with LPS at 48 hours after E. coli treatment results in augmented proinflammatory cytokine production in NF-kappaB-suppressed macrophages compared to control cells. We thus demonstrate that classical NF-kappaB activation inhibits autophagy and promotes delayed programmed cell death. This mechanism is likely to prevent the recovery of inflammatory cells and thus contributes to the resolution of inflammation.

Indexed as

AnimalsApoptosisAutophagyCell LineCells, CulturedCell SurvivalElectrophoretic Mobility Shift AssayEscherichia coliGene Expression ProfilingI-kappa B ProteinsInflammationMacrophage ActivationMacrophagesMiceMice, Inbred C57BLNF-kappa BI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouse

Identifiers

PMID18566685
PMCPMC2430012

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.